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Rockland Immunochemicals
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OriGene
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Addgene inc
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MedChemExpress
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Aviva Systems
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OriGene
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OriGene
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ABclonal Biotechnology
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Creative BioMart
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Image Search Results
Journal: Prostate cancer and prostatic diseases
Article Title: Discovery of a new candidate drug to overcome cabazitaxel-resistant gene signature in castration-resistant prostate cancer by in silico screening.
doi: 10.1038/s41391-021-00426-0
Figure Lengend Snippet: Fig. 2 AURKB and KIF20A as therapeutic targets of pimozide (PZD). A Venn diagram of genes upregulated in CBZ-resistant DU145CR and downregulated by PZD. B DAVID functional annotation clustering revealed genes related to cell division, chromatin cohesion, and kinetochore were downregulated by PZD. C Kaplan–Meier curves of recurrence-free survival in The Cancer Genome Atlas prostate cancer cohort by high or low AURKB expression. D Kaplan–Meier curves of recurrence-free survival according to KIF20A expression in The Cancer Genome Atlas prostate cancer cohort.
Article Snippet: Human overexpression lysates of
Techniques: Biomarker Discovery, Functional Assay, Expressing
Journal: Prostate cancer and prostatic diseases
Article Title: Discovery of a new candidate drug to overcome cabazitaxel-resistant gene signature in castration-resistant prostate cancer by in silico screening.
doi: 10.1038/s41391-021-00426-0
Figure Lengend Snippet: Fig. 3 AURKB / KIF20A expression in cabazitaxel-resistant prostate cancer cells. A AURKB and KIF20A mRNA expression in CBZ-sensitive DU145 and in DU145CR cells. B AURKB or KIF20A protein expression in LNCaP, DU145, DU145CR cells and overexpression lysates of AURKB or KIF20A. C Flow cytometry indicating the percentage of AURKB-positive cells is increased in DU145CR vs. DU145 cells. D KIF20A-positive cells are also increased in DU145CR cells.
Article Snippet: Human overexpression lysates of
Techniques: Expressing, Over Expression, Flow Cytometry
Journal: iScience
Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression
doi: 10.1016/j.isci.2025.113194
Figure Lengend Snippet: Correlation and impact of AURKB expression on TERT levels in thyroid cancer subtypes (A) Thyroid cancer cells transfected with AURKB-specific shRNA plasmids were harvested following 4-day puromycin selection for assessment of AURKB levels by western blotting and TERT by RT-qPCR. Plotted values are the mean ± SD of three independent experiments, each performed in triplicate, expressed as fold-change in normalized expression relative to untransfected control. (B–F) Correlation between TERT and AURKB expression determined by RT-qPCR in TERTp mutated thyroid tumor cell lines: TPC1 (PTC), SW1736, 8505C, and C643 (ATC), alongside the non-malignant NThy-ori-3.1 cell line. Correlation between TERT and AURKB expression in (C) 220 PTC samples from the TCGA study, and (D) 37 advanced thyroid cancers from the Landa et al. study, using z-scores calculated from available transcriptomic data. Quantitative ChIP of AURKB, EZH2 and H3S10ph, H3K4Me3 and H3K27Me3 epigenetic marks at specific regions spanning the TERT transcriptional start site. Chromatin was prepared from (E) mutant C643 or TPC1, and (F) wild-type CAL62 and MDAT-T41 cells treated for 24 h with either 180 nM Hesperadin or DMSO. Plotted values are the mean average ± SD of three independent experiments. For all experiments, asterisks (∗) denote significant changes, determined at p < 0.05, using an unpaired two-tailed t -test with the assumption of equal variances.
Article Snippet:
Techniques: Expressing, Transfection, shRNA, Selection, Western Blot, Quantitative RT-PCR, Control, Mutagenesis, Two Tailed Test
Journal: iScience
Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression
doi: 10.1016/j.isci.2025.113194
Figure Lengend Snippet: Impact of AURKB inhibition on TERT expression and telomerase activity (A–C) Dose response of TERT expression measured by RT-qPCR across thyroid cancer cell-lines treated with 0.1–10 μM Hesperadin. Plotted values are the mean ± SD of three independent experiments, each performed in triplicate, expressed as fold-change in normalized expression relative to DMSO control. Time-course analysis showing modulation of (B) TERT expression 24–72 h measured by RT-qPCR and (C) telomerase activity relative to MCF7 control 72–120 h measured by qTRAP, following treatment with IC50 dose of Hesperadin across various cancer cell lines. (D–F), Cell-cycle independent effect of Hesperadin on TERT expression was assessed by RT-qPCR at 0, 3, and 6 h post IC50 Hesperadin dose in SW1736 and CAL62 cells, which were arrested at the G2/M phase by Nocodazole. Flow cytometry was utilized to evaluate the cell cycle distribution of cells exposed to a 24 h Nocodazole vehicle, 24 h Nocodazole with a 6 h Hesperadin vehicle, or Nocodazole plus 6 h Hesperadin treatment. Data illustrates average cell percentages in G1, S, and G2/M phases (±SD). Values presented are mean ± SD from three independent experiments, each conducted in triplicate, expressed as fold changes in normalized expression/activity relative to 0 h baseline levels. For all experiments, asterisks (∗) denote significant changes, determined at p < 0.05, using an unpaired two-tailed t -test with the assumption of equal variances.
Article Snippet:
Techniques: Inhibition, Expressing, Activity Assay, Quantitative RT-PCR, Control, Flow Cytometry, Two Tailed Test
Journal: iScience
Article Title: AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression
doi: 10.1016/j.isci.2025.113194
Figure Lengend Snippet: mTORC1 inhibition leads to the dissociation of TRIM28-TRIM24 and AURKB from the mutant TERT promoter (A–F) Representative western blot images showing TRIM28 and TRIM24 expression across thyroid cell-lines. Co-immunoprecipitation of (B) endogenous TRIM24 in SW1736 and C643 cells; or (C) exogenous flag-tagged proteins overexpressed in SW1736 cells. Whole-cell lysates were incubated with anti-TRIM28 or IgG antibody for IP. (D, Left hand panel) Representative western blot images showing REST and expression across thyroid cell-lines. (D, Right hand panel) Co-immunoprecipitation of endogenous TRIM28 and AURKB by REST proteins in SW1736. Quantitative ChIP analysis was performed to measure TRIM28, TRIM24, AURKB, REST, EZH2 and H3S10ph levels at specific regions around the TERT transcriptional start site in (E) TPC1 and C643, and (F) CAL62 and MDAT-T41 cell following treatment with 2 nM Everolimus or DMSO for 6 h. The plotted values represent the mean ± SD derived from three independent experiments. In all experiments, asterisks (∗) indicate significant changes, determined at p < 0.05 using an unpaired two-tailed t -test with the assumption of equal variances.
Article Snippet:
Techniques: Inhibition, Mutagenesis, Western Blot, Expressing, Immunoprecipitation, Incubation, Derivative Assay, Two Tailed Test